We plan to continue gathering information (genetic control, physiological control, specific chemical inhibitors) on the growth medium dependent pathways of excision repair (i.e., those now known to be controlled by recA, recB, C, exrA, and polC), and on the different pathways of post-replicational repair (e.g., now known to be controlled by recB, C, exrA and uvrD; preliminary data from this laboratory) with special emphasis upon determining which of these pathways (and any new pathways that we may discover) are error free and which are error prone (i.e., mutagenic). This will necessitate determining mutation yields under experimental conditions known to modulate the different repair pathways.